ArticleCell death and differentiation2023
The embryonic patterning gene Dbx1 governs the survival of the auditory midbrain via Tcf7l2-Ap2δ transcriptional cascade.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Molecular and cell type-specific determinants of inferior colliculus development and auditory function.bioRxiv : the preprint server for biology · 2026Article
- HomozygousNeurology. Genetics · 2025Article
- Molecular Cascades That Build and Connect Auditory Neurons from Hair Cells to the Auditory Cortex.Journal of experimental neurology · 2025Article
- Impact of c-JUN deficiency on thalamus development in mice and human neural models.Cell & bioscience · 2024Article
- Harmony in the Molecular Orchestra of Hearing: Developmental Mechanisms from the Ear to the Brain.Annual review of neuroscience · 2024Review
- Article
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
At the top of the midbrain is the inferior colliculus (IC), which functions as the major hub for processing auditory information. Despite the functional significance of neurons in the IC, our understanding of their formation is limited. In this study, we identify the embryonic patterning gene Dbx1 as a key molecular player that governs genetic programs for IC survival. We find that Dbx1 plays a critical role in preventing apoptotic cell death in postnatal IC by transcriptionally repressing c-Jun and pro-apoptotic BH3 only factors. Furthermore, by employing combined approaches, we uncover that Tcf7l2 functions downstream of Dbx1. Loss of Tcf7l2 function causes IC phenotypes with striking similarity to those of Dbx1 mutant mice, which include defective embryonic maturation and postnatal deletion of the IC. Finally, we demonstrate that the Dbx1-Tcf7l2 cascade functions upstream of Ap-2δ, which is essential for IC development and survival. Together, these results unravel a novel molecular mechanism for IC maintenance, which is indispensable for normal brain development.
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